Our objectives are to 1) investigate the role of bulbospinal serotonin systems in the mediation of analgesia produced by narcotic analgesics; 2) study the possible interactions between noradrenergic and serotonergic systems in the brain stem and the involvement of this interaction in narcotic analgesia; 3) obtain additional evidence for the transmitter function of serotonin in the dorsal horn of the spinal cord; and 4) establish the pathways and synaptic sites at which serotonin acts as a neurotransmitter. We will test the hypothesis that narcotic analgesics such as morphine produce analgesia by directly or indirectly activating serotonin cells in the caudal brain stem which project to the spinal cord and presynaptically inhibit primary afferent terminals of fibers carrying pain impulses. BIBLIOGRAPHIC REFERENCE: Proudfit, H.K. and Anderson, E.G.: Morphine Analgesia: blockade by raphe magnus lesions. Brain Research 98: 612-618, 1975.